In vitro soluble cd30 levels in patients with chronic stable coronary artery disease

The CD30 antigen seems to play a costimulatory role in maintaining the physiological balance between T-helper [Th] l/Th2 immune responses. In this study, plasma and in vitro soluble CD30 [sCD30] secretion was investigated in patients with coronary artery disease [CAD] as a plausible marker of dysregulated immune response. Twenty one patients with angiographically confirmed CAD and 31 healthy controls took part in this study. The levels of the activation marker sCD30 were determined in plasma and phytohaemagglutinin [PHA]-stimulated and unstimulated peripheral blood mononuclear cell cultures by ELISA. Plasma sCD30 levels did not differ significantly between the patients and controls. However, spontaneous sCD30 secretion was significantly lower in patients with CAD compared to controls [p < 0.001]. The soluble CD30 levels were significantly increased in the supernatant of PHA-stimulated PBMCs compared to unstimulated cultures in both groups of patients and controls [p < 0.001]. PHA-stimulated sCD30 secretion was found to be lower in patients compared to controls; however, the difference was not statistically significant. Plasma sCD30 levels were not statistically different in patients with chronic stable CAD, a well-known Thl-mediated disease, compared to controls; whereas decreased spontaneous and PHA-stimulated sCD30 secretion in patients with CAD might indicate the progressive shift towards a Thl immune response

Lymphocyte cytotoxicity of oxLDL in patients with atherosclerosis

Atherosclerosis, a chronic inflammatory disease of the vessel wall is characterized by local and systemic immune responses to a variety of antigens. Oxidized low-density lipoprotein [oxLDL] is considered as an important determining factor in the pathogenesis of atherosclerosis. The purpose of this study was to investigate the degree of peripheral blood mononuclear cells [PBMC] vulnerability to in vitro oxLDL-induced cytotoxicity from atherosclerotic patients in comparison to healthy individuals. Thirty patients with atherosclerotic lesions, confirmed by angiography, and 30 matched healthy individuals were investigated. PBMC was prepared from individuals' blood samples which were further stimulated with low dose [1 micro g/mL] and high dose [50 micro g/mL] of extensively oxidized LDL. MTT assay was utilized to measure cell viability and proliferation. Stimulation index [SI] was calculated as mean ratio of optical density [OD] of the stimulated cells divided by OD of untreated cells. Low dose oxLDL treatment caused no significant proliferative or cytotoxic effect in the control group; however, similar treatment caused significant cytotoxic effect in the patient group compared to the controls [p=0.026]. High dose oxLDL treatment induced more significant cytotoxicity in the patient compared to the control group [p=0.006]. Comparison of the SI between the two groups of patients and controls showed significantly lower index by either the low [p=0.03] or the high dose [p<0.001] oxLDL in the patients compared to the controls. PBMC from patients with atherosclerosis showed increased susceptibility to oxLDL-induced cytotoxicity. Our results imply that prolonged exposure to elevated levels of circulating oxLDL could weaken the cellular defense mechanisms by progressive depletion of the pool of antiapoptotic proteins, rendering the cells more vulnerable to oxLDL-induced cell death